Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.2 (focal adhesion kinase)
44,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human mixed leukocyte supernatants contain thymocyte proliferative activity (TPA) and a low m.w. helper factor, designated HP-1, which is capable of partially restoring the antibody response of T-cell-deficient adherent murine spleen cells to the thymic-dependent antigen, SRC. TPA and HP-1 appear to have a comparable m.w. (14,000 to 14,500 daltons) by Sephadex gel filtration column chromatography. Furthermore, HP-1 and TPA exhibit similar patterns of heterogeneity on DEAE-cellulose chromatography, elute together on CM-cellulose chromatography, and manifest identical patterns of migration on polyacrylamide gel electrophoresis. These data suggest that the TPA and HP-1 activities reside in either the same molecule(s) or in different molecules with identical charge/mass ratios. Furthermore, the results support the hypothesis that the helper activity of HP-1 is derived from its capacity to activate T and/or pre-T cells.
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PMID:Association of a low molecular weight helper factor(s) with thymocyte proliferative activity. 30 39

The B-cell mitogens LPS and lipoprotein stimulate 20-35 percent of all B cells in the spleen of 6- to 8-wk old C3H/Tif mice, as determined by limiting dilution analysis of precursors. Each reactive cell grows to a clone of IgM-secreting PFC, enumerated in a hemolytic plaque assay detecting all IgM secreting cells, regardless of v-region specificity. We have used these mitogens to reveal the total repertoire of Ig specificities produced by these mitogen-reactive B cells. We have determined in plaque assays with six different target erythrocytes the number of spleen cells limiting to one the number of mitogen-reactive B cells detected as specific IgM-secreting clones in each of these plaque assays. By this method, the absolute frequencies of precursor B cells with defined v-gene specificities could be calculated, for at least, one third of all B cells. The frequencies of specific IgM-plaque-forming B-cell clones within the total pool of mitogen-reactive B cells was 1 in 10 for NIP(12),-SRC, 1 in 50 for TNP(12)- SRC, 1 in 100 for NIP(1)-SRC, 1 in 160 for TNP(3)- SRC, 1 in 500 for HRC, and 1 in 1,000 for SRC. These frequencies were the same in the LPS- and in the lipoprotein-reactive B-cell population for TNP(30)- SRC and SRC.
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PMID:Frequencies of mitogen-reactive B cells in the mouse. II. Frequencies of B cells producing antibodies which lyse sheep or horse erythrocytes, and trinitrophenylated or nitroiodophenylated sheep erythrocytes. 32 69

While rheumatoid-factor-producing haemolytic plaque-forming cells (RF--PFC) of the human peripheral blood were easily inhibited by cycloheximide, mouse spleen cells immune to sheep red cells (anti-SRC PFC) were inhibited only after prolonged preincubation in the drug. The RF--PFC were easily inhibited by propranolol, while the anti-SRC PFC were not at all inhibited. Vinblastine inhibited both systems equally. These differences are taken to suggest that the RF--PFC have very little preformed antibody in them and therefore depend upon active protein synthesis for their demonstration. In contrast, anti-SRC PFC, which may be predominantly mature plasma cells, generally need no new protein synthesis for their demonstration because of increased quantities of preformed antibody. A possible mechanism is that RF--PFC may represent primarily RF-specific B cells, the RF of which is released by surface immunoglobulin shedding and therefore susceptible to membrane stabilising agents such as propranolol.
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PMID:Metabolic inhibition of plaque-forming cells: comparison of human rheumatoid-factor-producing cells with mouse anti-sheep erythrocyte-producing cells. 38 30

2-methyl-3(3'-methyl-2'-pyridyl)-4 (3H) quinazolinone (SRC-820) and methaqualone inhibited the growth of Streptococcus faecalis-R (ATCC-8043). Phosphoenolpyruvate formation from 3-phosphoglycerate by an enzyme extract of S. faecalis was inhibited by SRC-820. With edetate or fluoride, an additive inhibitory effect by SRC-820 was observed.
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PMID:Effect of a quinazolinone derivative on the metabolism of Streptococcus faecalis--R (ATCC-8043). 40 53

Sheep erythrocytes were pretreated with concanavalin A (Con-A-SRC), or glutaraldehyde (G-SRC), or specific rabbit immunoglobulin G (IgG-SRC), or specific rabbit immunoglobulin M and complement (C-SRC). Each erythrocyte type was made to adhere to rat peritoneal cells and adhesion was measured; binding decreased as follow: conA-SRC greater than IgG-SRC greater than less than G-SRC greater than C-SRC Peritoneal cell-erythrocyte complexes were then submitted to a laminar shear flow, and resistance of binding was assayed. Binging strength decreased in the following order: G-SRC greater than C-SRC greater than IgG-SRC greater than ConA-SRC Cell suspensions were incubated at 37 degrees, and phagocytosis was measured. Ingestion decreased in the following order: G-SRC greater than IgG-SRC greater than C-SRC greater than ConA-SRC It is concluded that: Binding strength may be of importance in triggering phagocytosis; when immunocytoadherence is studied, two independent parameters should be considered: binding and binding strength. This report describes a new method that may allow discrimination between different cell subpopulations of similar binding specificities.
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PMID:Dependence of phagocytosis on strength of phagocyte-particle interaction. 68 Aug 1

Heavy trinitrophenylated sheep red cells (TNP128SRC) and glutaraldehyde-treated SRC (G-SRC) could not induce cellular cytotoxicity against 51Cr-SRC. In contrast, the native antigen SRC could stimulate a cytolytic response against the radiolabeled homologous target cell. However, fixed SRC could stimulate a priming function that accelerated and augmented the secondary cytotoxic response to SRC. Such fixed antigens could stimulate a delayed-type hypersensitivity (DTHS) response also. Thus, the immunologic memory to the chemically modified antigen, as well as the DTHS response, are completely dissociated from the primary cytotoxic responses. The primary and the secondary cytotoxic responses that were developed in the spleens of the injected mice were mediated by antibody-dependent cellular cytotoxicity (ADCC), since the active supernatant that was released from the spleen cells could lyse the target cells in the presence of normal splenocytes. The active supernatant was identified as antibody. We suggest that B effector cells cytolyzed the antibody-coated target cells. Normal cells from nude mice could mediate the cytolytic process as efficiently as spleen cells from other strains of mouse. The results are discussed in terms of selective stimulation of T cell subpopulations.
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PMID:Studies on the immune response to fixed antigens. III. Induction of helper function for antibody-dependent cellular cytotoxicity responses. 68 40

SRC-3605, N-N-bis-P-chlorophenyl 3-p-tolyl glutaric acid diamide, was studied for its hypocholesterolaemic effect on serum and liver cholesterol in hypercholesterolaemic weanling and adult female rats. Weanlings were administered doses of SRC-3605 ranging from 100 to 300 mg/kg body weight for 4 or 8 consecutive days. The greatest hypocholesterolaemic effect was observed with doses of 150, 200 and 250 mg, although a progressive decreases in serum cholesterol was noted with increasing doses. Hepatic cholesterol decreases supported the serum data, but were inconsistent. Hypercholesterolaemic adult animals received 50, 100, 150 or 200 mg/kg body weight of either SRC-3605 or clofibrinic acid for 4 days. A decrease in serum cholesterol levels was observed only with the 200 mg SRC-3605. No clear-cut influence of the either compounds was found on hepatic cholesterol. The results indicated that SRC-3605 possesses the property to reduce both serum and liver cholesterol in hypocholesterolaemic weanling female rats.
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PMID:Effectiveness of N-N-bis-P-chlorophenyl-3p-tolyl glutaric acid diamide (SRC-3605) as a hypocholesterolaemic compound in hypercholesterolaemic female weanling and adult rats. 72 Dec 49

Mice of 1.5, 9, 22, and 31 to 32 months of age were injected with the thymus-dependent antigen, TNP-SRC, or the thymus-independent antigen, TNP-SRC, TNP-MRC. The anti-SRC and TNP immune responses to TNP-SRC were markedly reduced in older mice, whereas the anti-TNP response to the TNP-MRC showed no substantial decline. Young mice produced higher anti-TNP plaque-forming cell responses after injection of TNP-SRC than after TNP-MRC, whereas in older mice the reverse obtained. Old mice but not young mice displayed a high anti-SRC cross-reactive response after injection of TNP-MRC. The avidity of anti-TNP antibody of young mice immunized with TNP-SRC was higher than that following immunization with TNP-MRC, whereas the avidities of anti-TNP antibodies from old mice injected with these two reagents were the same. Those individual mice which showed a poorly regulated immune response also displayed an autologous anti-MRC plaque-forming cell response after injection of either TNP-SRC or TNP-MRC. It is suggested that mechanisms mediated by suppressor T cells may be responsible for regulating the autoimmune response to modified self antigens, and that these are severely impaired in age individuals.
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PMID:Autoimmunity and aging: the age-related response of mice of a long-lived strain to trinitrophenylated syngeneic mouse red blood cells. 79 42

Mice primed with heavily trinitrophenylated sheep red cells (TNP128SRC) or glutaraldehyde-treated sheep red cells (G-SRC) developed an early helper function mediated by thymus-derived cells. Such mice were able to produce high secondary responses to both hapten and carrier after challenge 2 days after priming, with lightly trinitrophenylated SRC (TNP0.14SRC). However, the primary response of the TNP128SRC or G-SRC-primed mice were very low to undetectable, and their secondary responses were also low when the challenge antigen was administered 4 days after priming or later. Inhibitory humoral factor(s) which were induced in the primed animals appeared responsible for the decreased capacity of primed mice to mount a secondary response when challenged later than 2 days after priming. Transfer of spleen cells from TNP128SRC-primed mice to sublethally irradiated recipients circumvents their exposure to inhibitory humoral factor(s) present in intact animals allowing them to react with challenge antigen. Enriched populations of T cells, but not B cells, were able to transfer this early immunologic memory to irradiated recipients. The theoretical and practical implications of these results are discussed.
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PMID:Studies on the immune response to fixed antigens. Preferential induction of helper function with heavily trinitrophenylated sheep erythrocytes, and glutaraldehyde-treated sheep erythrocytes. 81 79

IgM and IgG anti-sheep red blood cells agglutinins were measured from dayy + 2 to day + 30 in SPF mice immunized with 108 SRC and treated with 2.5 or 25 mg LMS/dg. Untreated control mice produced high levels (1:8200) of IgM-antibodies from day + 4 to day + 20. Early, day + 4, IgG-agglutinins appeared together with IgM-antibodies in mice treated with 2.5 mg LMS/kg, whereas administration of 25 mg LMS/kg induced the synthesis of antibodies belonging only to the IgG class. Titres were significantly lower (1:512) in LMS-treated mice than in controls. The switch to IgG of antibody formation is another for the ability of LMS to stimulate T cell activities.
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PMID:[Influence of levamisole on antibody production]. 84 84


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